Year : 1983 | Volume
: 31 | Issue : 7 | Page : 1005--1009
Pathogenesis and photocoagulation of subretinal neovascular membranes
Pater H Morse
Department of Ophthalmology and the Eye Research Laboratories, The University of Chicago Pritzker School of Medicine, Chicago, Illinois, USA
Pater H Morse
Department of Ophthalmology and the Eye Research Laboratories, The University of Chicago Pritzker School of Medicine, Chicago, Illinois
|How to cite this article:|
Morse PH. Pathogenesis and photocoagulation of subretinal neovascular membranes.Indian J Ophthalmol 1983;31:1005-1009
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Morse PH. Pathogenesis and photocoagulation of subretinal neovascular membranes. Indian J Ophthalmol [serial online] 1983 [cited 2021 Sep 22 ];31:1005-1009
Available from: https://www.ijo.in/text.asp?1983/31/7/1005/29730
Subretinal neovascular membane; (SRNVM's) may be single or multiple and arf likely to occur as a secondary complication o idiopathic or known diseases damaging the retinal pigmented epithliu m and Bruch's membrane. Predisposing factors are a dehis. cence in Bruch's membrane, physical deformity of anatomical boundaries, and conceivable focal ischemia. S1.NVM forma. tion may be further enhanced by the phagocytosis, lysosomal activity, or enzymatic lysis of tissues by macrophages or lymphocytes.
SRNVM's have been observed idiopathically in both young and old pati,enlts. They are also seen in patients with senile (exudative) macular degeneration, presumed ocular his. toplasmosis syndrome, severe nnyopia, chorioretinal atrophy resulting from healed disseminated chorioretinitis of unknown etiology, toxoplasmossi, toxocariasis., sarcoidosis, drusen of the optic nerve head hereditary drusen of Bruch's membrane angioid streaks, pseudotumor cerbri, chor oidal folds, Best's vitelliruptive macula degeneration, fundus flavimaculatus, rubells choroidal nevi, choroidal melanomata, choroidal hemangiomata. hamartomas of the retinal pigmented epithelium, metastatic tumors, coccidioidomycosis, Harada's disease, acute multifocal posterior placoid pigment epitheliopathy, Behcet's disease, geographic helicoid (serpiginous) choroiditis and choroidal rupture. SRNVM's may also occur after excessively intense photocoagulation.,,,,,,,,,,,.
The location of a SRNVM is of critical importance not only with inspect to the symptoms experienced by the patient, but also with respect to the potential for treatment. The commonest location for symptomatic lesions are paramacular, macular, or juxtapapillary.
The clinical appearance of SRNVM's is widely variable often depending upon the manifestations of the underlying disease.
Any patient over 45 years of age with the symptoms and signs of a disease resembling central serous choroidopathy should rouse suspicion as showing manifiestations of the very earliest SRNVM. A serous or hemorrhagic elevation of the retinal pigmented epithelium or sensory retina often is an early manifestation of a SRNVM before it has enlarged to a sufficient size to be discernible either by ophthalmoscopy or flourescein angoiography. The serous or hemorrhagic elevations of the retinal pigmented epithelium may appear gray-brown, gray-green, or yellow-pink color. On occasion, the elevation ni y have no alteration in color. Frequently there is a marginal subsensory retinal hemorrhage which after it breaks through the retinal pigmented epithelium is red in color. Almost invariably the SRNVM islocated beneath the gray - green or yellow - pink collored lesions. The ophthalmoscophc of the growth and natural history of a SRNVM are quite characteristic. The presence of a SRNVM located beneath the foveola, even without serous transudation or hemorrhage, may compromise the metabolism and function of the photoreceptors and retinal pigmented epithelium which are essential for central vision. The buds of capillaries initiating SRNVM growth usually originate from the choriocapillaris but occasionally have been described as coming from the choriocapillaris but occasionally have been described as coming from larger choroidal vessels and are accompanied by mesenchymal fibrous tissue. In the initial phases the vascular component is predominant and transudes plasma or hemorrhages.
The early stage is superceded by intermediate or chronic phase in which the vascoular tissue involutes and the fibrous component opacifies becoming more visible. In the stages of transudation and hemorrhage, the retinal pigmented epithelium and sensory retina may be elevated either by plasma or hemorrhage. Intermediate to chronic manifestations may be represented by subretinal hemorrhage, resorbing subretinal hemorrhage which is often yellow in color, hard yellow exudates in the retina, cholesterol crystals, subretinal fibrosis, chorioretinal atrophy, clumping of melanin granules, areas of hypo and hyperigmentation, chronic serous separation of the central retina and overlying cystoid macular edema. Hemorrhage from a SRNVM may break through into the vitreois obscuring fundus details. In the chronic stages one observes subretinal fibrosis, which is largely the residual mesenchymal tissue accompanying the growth of the neovascular component. Some subretinal fibrosis nay be the result of metaplasia of the reinal pigmented epithelium. The smaller retrial vessels in teh fibrous tissue transude serous fluid wich may lead to a chronic separation of the central retina. This chronic serous of sometimes hemorrhagic separation of thesensory retina predisposes to continuous atophy of the photoreceptors and a deleterious effect on the retinal pigmented epithelium. As a consequence of chronic serous separation of the retina there may also be dilation and tortuosity of the overlying retinal vessels.,,,,,,
One of tie indications for fluorescein angiography is to delineate the extent of a SRNVM. Flourescein angiography is not a diagnostic nodality, but rather one which is useful as a gulideline in the application of photocoajulation. Hemorrhage or turbid subretioml fluid may also obscure the ouline of the SRNVM on the fluorescein angiograph. In the early stages of the development when the vasclar component is predominant and the SRNVW has attained a sufficient size to be deeinel by fluourescein angiography, a charrcterstic lacy pattern appears in the earl, phases of fluorescein angiorgraphy. In theater stages of fluorescein angiography the details of the vascular patterns are obscured by extravisation of the fluorescein dye. In the late phases of the natural history of the SRNV, when the fibrous tissue predominates, fluoresces angiography reveals a staining or low Bade leking from the very small ophthaltmscopically invisible blood vessels it the fibrous tissue. Fluorescein angiograpiy is of no value in an eye in which theSRNVM appers in its final stage and in whch the visual acuity is unrestorable by treatment. Fluorescein angiography should be done on the eye with better vision or more acute manifestations of a SRNVM in the hope of being able to apply treatment at a more favorable time. Once photocoagulation has been applied, a fluorescein angiogram immediately following treatment is of little value because the hyperfluorescence and staining is intensified, often blurring fine detail making interpretation impossible. Fluorescein angiograms to determine the obliteration of the SRNVM, if they are necessary, should be otained 7-14 days following photocoagulation when healing has begun,. Photocoagulation is currently the most effective therapeutic modality to obliterate SRNVM's. The success of the therapy and the final vision in the patient, will depend upon the location, size, and amount of secondary damage such as disruption of the integrity of the retinal pigmented epithelium or the presence of chronic serous separation of the macula created by the SRNVM both of which may additionally damage the photoreceptors.
A good quality fluorescein angioram may be used as a guide during photocoagulation. Frequently the outlines of lesions are not seen with good definitation ophthalmoscopically or using the slit-lamp and contact lens. In such cases the retinal vascular pattern on the fluorescein angiogram may be used to delineate the extent of the SRNVM when a patient is photocoagualted. Any modality of photocoagulation may be used in treatment, including the Xenon arc, Argon, or Krypton lasers. However, in lesions close to the foveloa, the choice of wavelength is quite important. The blue wavelength of the Argon laser are quite deleterious as they are absorbed by xanthophy 11. The green wavelength of the Argon laser and the red wavelength of the Krypton laser are the most useful and effective. The red wavelengths of the Krypton laser penetrate to the deeper layers from wherce SRNVM s originate they also are not absorbed by hemorrhage,,. Greater absorption of certain wavelengths by hemorrhage may lead to a conduction of the thermal effect of the photocoagulation which will create more damage to adjacent tissues. Commonly, in the months to years after photocoagulation, the size of the resulant spot of chorioretinal atrophy enlarges. this may reduce central visual acuity if the pigmented epithlium beneath the foveloa is damaged. Also, it must be remembered that any wavelength, if applied directly to retinal pigmented epithelium beneath the foveola will decrease the patient's vision. The intensity of the photocoagulation must be adjusted, using three variables, spot size duration of exposure, and power to ensure adequate but not excessive treatment. It has been found that heavy or intense treatment originally advocated for the treatment of SRNVM's is frequently not needed. Often two to three treatments of a lighter intensity will be better than one heavy treatment. Laser burns spread to a greater extent if there is an increase in either the powere or duration of the treatment time. If the duration of the treatment time is shortened to less than 0.1 second the greater impact may create a rupture of retinal or choroidal vessels.
Using a 50 or 100 micron spot size, one outlines the extent and location of the SRNVM. An area of uninvolved tissue surrounding the outlined SRNVM should also be lightly treated. Once the SRNVM has been delineated the spot size may be enlarged to 200 or 500 microns and the central portion of the SRNVM photocoagulated.
The treatment spot size, which is the attenuated laser beam, should be focussed at the level of the lesion being treated. This is particularly true when there is overlying subretinal fluid and the beam should be focused on the SRNVM underlying the secondary serous separation. When one is treating juxtapapillary SRNVM's lying beneath the papillomacular bundle overlying subretinal fluid is beneficial for its insulating effect. The treatment should not create a white reaction in the retina within the papillomacular bundle.
The reaction to the laser should be gray to gray-white in color. If a Krypton laser is used an adequate lesion is obtained is obtained with a less visible reaction. As the acute lesion created by the laser heals, it is replaced by a variable amount of chorioretinal atrophy with hypo and hyperpgmentation. The appearance of a gray-green or yellow-pink colored elevation at the margin of the chorioretinal atrophy signifies a recurrence of the SRNVM and is an indication for immediate retreatment.
Patients should be examined weekly for one month following photocoagulation. Thereafter they should be seen every three to six months or annually _depending upon whether or not they have-a disease predisposing to further SRNVM growblt: Adequate and successful treatment with photocoagulation limits the size of a SRNVM and aborts its growth potential. The natural history of the, process is accelerated by photocoagulation which obliterates the vascular component aitd leaves residual fibrosis. If photocoagulation is used on smaller SRNVM's in the earlier stages the resultant scotoma will be smaller and the amount of subretinal fibrosis, which increases in size as the SRNVM grow, will be minimized. With satisfactory obliteration of neovascularization the risk of hemorrhage and chronic serous fluid transudation is also eliminated,,,,,.
Inadequte, imcomplete, or excessive treatment may cause failure. Ther may be regrowth of the $RNVM from within the area which was photocoagulated, at its margin, and elswehere, particularly in a patient with a predisposing disease such as senile macular degeneration. Excessive photocoagulation creates chorioretinal atrophy and dehiscences in Bruch's membrane which may predispose to the appearance fo another SRNVM. Excessive impact of the laser beam especially when using shorter duration of exposure and higher powere may cause a rupture of retinal or choroidal vessels. Prior to the healing of the lesion created by the laser there is often a greater amount of transudate of edema which may temporarily decrease visual acuity. if the amount of fibrous tissue in the SRNVM is large its contraction during the healing process may create folds or striae in the retina. If these folds or striae affect the foveola, there may be a decrease in central visual acuity and the patient may experience metamorphosia. Photocoagulation may also create scotomata or sectoral visual field defects, depending upon the location and intensity of its application. Other complications of photocoagulation include damage to the cornea, lens, and iris. These are quite rare and may be avoided by careful treatment. Combined or chroidal sparation is sometimes seen as a complication of rather extensive photocoagulation and preretinl or vitreoretinal membranes have also been noted usually after heavy photocoagulation.
The natural history of SRNVM's is unpredictable with respect to their appearance, rapidity of growth, and ultimate size.
The symptoms may not be noticed by the patient until the SRNVM has extended beneath the foveola making effective treatment quite difficult if not imposible.
SRNVM's that occur in areas that are quite safe for treatment may undergo spontaneous involution in their natural history without therapy.
However, it is impossible to predict at this time which patients will have this favorable outcome and hich will be jeopardized or lose central visual acuity by the enlargement of these membranes. Even in patients who are well informed intelligent, and aware of their condition, a rapid enlargement of a SRNVM may threaten or destroy central vision. The ultimate prognosis depends upon the location of the lesion, the efficacy of the treatment, and the secondary changes caused by the complication of SRNVM growth or the underlying disease which predisposses to such neovasuclarization.
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